The original hygiene hypothesis has been revised, suggesting that deficient regulatory mechanisms are responsible for the rising trends in inflammatory disorders. Helminths establish long-lived chronic infections in their definitive host, with avoidance and manipulation of host effector response. Throughout helminth infections, immunoregulatory networks are generated, limiting immunopathology and permitting survival of parasites. I propose that helminth induced regulatory networks extend to regulate damaging allergic and autoimmune inflammatory responses. This thesis aimed to experimentally dissect the relationship between helminth infections and allergic diseases. We show here that cellular populations generated during a helminth infection can control both Th1-mediated autoimmune, and Th2-associated allergic inflammation. CD4⁺CD25⁺ T cells or CD19⁺ B-cells from mesenteric lymph nodes (MLN) of mice chronically infected with Heligmosomoides polygyrus were transferred to allergen sensitive or myelin oliogodenodrocyte glycoprotein (MOG) _(p35-55) immunised recipients. Allergen-sensitive mice receiving cells from infected donors had significantly reduced airway eosinophilia, broncho-alveolar lavage (BAL) fluid IL-5 and eotaxin secretions upon airway challenge in a model of allergic airway inflammation. Similarly, MOG_(p35-55) immunised mice receiving CD19⁺ B-cells from infected mice, had a significantly delayed onset and reduced severity of disease with fewer CD4⁺IFN-γ⁺ cells in the central nervous system (CNS) during experimental allergic encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). I propose a testable regulatory model encompassing multidimensional infectious tolerance with an array of regulatory cells. Taken together, these data highlight the immunoregulatory potential of chronic helminth infections, explaining the inverse relationship between helminth infections and dysregulated inflammatory events.